Abstract
ObjectiveTo determine the human dose‐response relationship between a stepwise increase in arterial oxygen tension and its associated changes in DO2 and sublingual microcirculatory perfusion.MethodsFifteen healthy volunteers breathed increasing oxygen fractions for 10 minutes to reach arterial oxygen tensions of baseline (breathing air), 20, 40, 60 kPa, and max kPa (breathing oxygen). Systemic hemodynamics were measured continuously by the volume‐clamp method. At the end of each period, the sublingual microcirculation was assessed by SDF.ResultsSystemic DO2 was unchanged throughout the study (P slope = .8). PVD decreased in a sigmoidal fashion (max −15% while breathing oxygen, SD18, P slope = .001). CI decreased linearly (max −10%, SD10, P slope < .001) due to a reduction in HR (max −10%, SD7, P slope = .009). There were no changes in stroke volume or MAP. Most changes became apparent above an arterial oxygen tension of 20 kPa.ConclusionsIn healthy volunteers, supraphysiological arterial oxygen tensions have no effect on systemic DO2. Sublingual microcirculatory PVD decreased in a dose‐dependent fashion. All hemodynamic changes appear negligible up to an arterial oxygen tension of 20 kPa.
Highlights
Supplemental oxygen is administered to patients with arterial hypoxemia to ensure sufficient oxygen delivery (DO2) to organs
The main finding of this study is that in healthy volunteers, supplemental oxygen does not alter DO2, while sublingual perfused vascular density (PVD) decreased in a sigmoidal fashion as arterial partial pressure of oxygen (PaO2) was increased stepwise from 14 up Intervention (n = 15) Target PaO2 fraction of inspired oxygen (FIO2) (%)
We found a significant reduction in sublingual PVD simultaneous to a stepwise increase in PaO2 in this group of healthy individuals
Summary
Supplemental oxygen is administered to patients with arterial hypoxemia to ensure sufficient DO2 to organs. Potential adverse effects of hyperoxia may occur via microvascular constriction[11,12] and a reduction in cardiac output.[13-16]. As with most studies on hyperoxia, only 2 inspired oxygen concentrations were studied; air (21% O2) and pure oxygen (100%) This comparison creates the highest contrast, its clinical relevancy is limited. The relation between hemodynamic effects of oxygen and PaO2 at clinically relevant doses remains unknown. A few groups investigated the dose-response effect of oxygen on the cardiovascular system[15,26] and none directly visualized the microcirculation It is currently unknown at which PaO2 the microcirculatory effects of hyperoxia start to occur and what the nature of the dose-response effect is. The aim of this study was to determine the dose-response relationship between a stepwise increase in PaO2 and its associated changes in DO2 and sublingual microcirculatory perfusion
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